GLA and Fabry disease: Males with pathogenic GLA mutations have practically no residual α-Gal activity and develop classical FD with the onset of symptoms (dysesthesia, gastrointestinal disorders, angiokeratomas, autonomous dysfunction) in childhood and, as we age, the risk of developing life-threatening complications involving vital organs, including progressive renal failure, stroke and hypertrophic cardiomyopathy with myocardial fibrosis and arrhythmias is increasing [25–29].